Ming Gao1, Hui Yan2, Rong-Hua Yin3, Qiang Wang4, Yi-Qun Zhan3, Miao Yu3, Chang-Hui Ge3, Chang-Yan Li3, Xiao-Hui Wang3, Zhi-Qiang Ge5, Xiao-Ming Yang6. 1. Tianjin University, Department of Pharmaceutical Engineering, Tianjin 300072, China; Beijing Institute of Radiation Medicine, Beijing 100850, China. 2. Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. 3. Beijing Institute of Radiation Medicine, Beijing 100850, China; State Key Laboratory of Proteomics, Beijing 100850, China. 4. Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China. 5. Tianjin University, Department of Pharmaceutical Engineering, Tianjin 300072, China. 6. Tianjin University, Department of Pharmaceutical Engineering, Tianjin 300072, China; Beijing Institute of Radiation Medicine, Beijing 100850, China; State Key Laboratory of Proteomics, Beijing 100850, China. Electronic address: xiaomingyang@sina.com.
Abstract
BACKGROUND & AIMS: Hepassocin (HPS) is a hepatotrophic growth factor that specifically stimulates hepatocyte proliferation and promotes liver regeneration after liver damage. In this paper, zebrafish were used to investigate the role of HPS in liver development. METHODS AND RESULTS: During zebrafish development, HPS expression is enriched in liver throughout hepatogenesis. Knockdown of HPS using its specific morpholino leads to a smaller liver phenotype. Further results showed that the HPS knockdown has no effect on the expression of the early endoderm marker gata6 and early hepatic marker hhex. In addition, results showed that the smaller-liver phenotype in HPS morphants was caused by suppression of cell proliferation, not induction of cell apoptosis. CONCLUSIONS: Current findings indicated that HPS is essential to the later stages of development in vertebrate liver organogenesis.
BACKGROUND & AIMS:Hepassocin (HPS) is a hepatotrophic growth factor that specifically stimulates hepatocyte proliferation and promotes liver regeneration after liver damage. In this paper, zebrafish were used to investigate the role of HPS in liver development. METHODS AND RESULTS: During zebrafish development, HPS expression is enriched in liver throughout hepatogenesis. Knockdown of HPS using its specific morpholino leads to a smaller liver phenotype. Further results showed that the HPS knockdown has no effect on the expression of the early endoderm marker gata6 and early hepatic marker hhex. In addition, results showed that the smaller-liver phenotype in HPS morphants was caused by suppression of cell proliferation, not induction of cell apoptosis. CONCLUSIONS: Current findings indicated that HPS is essential to the later stages of development in vertebrate liver organogenesis.